Metabolomic analysis reveals altered sphingolipid pathways in silicosis patients, suggesting potential biomarkers and therapeutic targets.
Silicosis is a fibrotic lung disease caused by the inhalation of crystalline silica. This study investigates sphingolipid metabolism in silicosis patients using plasma samples. GC-MS-based untargeted metabolomics identified alterations in the sphingolipid pathway, while LC-MS targeted specific ceramide and sphingomyelin species. Enzyme activities of acid ceramidase, neutral sphingomyelinase, sphingosine kinase-1, and sphingosine-1-phosphate lyase-1 were also assessed. Results showed elevated sphingolipid levels and reduced enzyme activities in patients versus controls. In silico molecular docking suggested interactions between SiO₂ and pathway enzymes. Metabolomic analysis revealed disrupted sphingolipid and fatty acid pathways. These findings highlight the role of sphingolipid dysregulation in silicosis pathogenesis and suggest its potential as a biomarker and therapeutic target. Understanding these mechanisms could improve management and treatment strategies for this debilitating disease.
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Aksu et al. (2025) studied this question.
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